Caffeine dependence is a condition characterized by a set of criteria, including tolerance, withdrawal symptoms, persistent desire or unsuccessful efforts to control use, and continued use despite knowledge of adverse consequences attributed to caffeine.[1] It can appear in physical dependence or psychological dependence, or both. Caffeine is one of the most common additives in many consumer products, including pills and beverages such as caffeinated alcoholic beverages, energy drinks, pain reliever medications, and colas. Caffeine is found naturally in various plants such as coffee and tea. Studies have found that 89 percent of adults in the U.S. consume on average 200 mg of caffeine daily.[2] One area of concern that has been presented is the relationship between pregnancy and caffeine consumption. Repeated caffeine doses of 100 mg appeared to result in smaller size at birth in newborns. When looking at birth weight however, caffeine consumption did not appear to make an impact.[3]
Moderate physical dependence often arises from prolonged long-term caffeine use.[4] In the human body, caffeine blocks adenosine receptors A1 and A2A.[5] Adenosine is a by-product of cellular activity: the stimulation of adenosine receptors produces feelings of tiredness and a drive for sleep. Caffeine's ability to block these receptors means the levels of the body's natural stimulants, dopamine and norepinephrine, continue at higher levels.
Continued exposure to caffeine prompts the body to create more adenosine-receptors in the central nervous system, which increases the body's adenosine sensitivity. This reduces the stimulatory effects of caffeine by increasing tolerance. It also causes the body to suffer withdrawal symptoms (such as headaches, fatigue, and irritability) if caffeine intake decreases.[6]
Pathologically reinforced caffeine use induces a dependence syndrome, but not an addiction.[8] For a drug to induce an addiction from repeated use at sufficiently high doses, it must activate the brain's reward circuitry, particularly the mesolimbic pathway.[8] Neuroimaging studies of preclinical and human subjects have demonstrated that chronic caffeine consumption does not sufficiently activate the reward system, relative to other drugs of addiction (e.g., cocaine, morphine, nicotine).[9][10][11] As a consequence, compulsive use (i.e., an addiction) of caffeine has yet to be observed in humans.[8] Caffeine dependence forms due to caffeine antagonizing the adenosine A2A receptor,[12] effectively blocking adenosine from the adenosine receptor site. This delays the onset of drowsiness and releases dopamine.[13] As of right now, caffeine withdrawal qualifies as a psychiatric condition by the American Psychiatric Association, but caffeine-use disorder does not.[14]
Professor Roland R. Griffiths, a professor of neurology at Johns Hopkins in Baltimore, strongly believes that caffeine withdrawal should be classified as a psychological disorder.[15] His research suggests that withdrawal affects 50% of habitual coffee drinkers, beginning within 12–24 hours after cessation of caffeine intake, and peaking in 20–48 hours, lasting as long as 9 days.[16][17] In another study, he concluded that people who take in a minimum of 100mg of caffeine per day (about the amount in one cup of coffee) can acquire a physical dependence that would trigger withdrawal symptoms, including muscle pain and stiffness, nausea, vomiting, depressed mood, and other symptoms.[15][6]
Physiological effects
Caffeine dependence can cause a host of physiological effects if caffeine consumption is not maintained. Commonly known caffeine withdrawal symptoms include headaches, fatigue, loss of focus, lack of motivation, mood swings, nausea, insomnia, dizziness, cardiac issues, hypertension, anxiety, and backache and joint pain; these can range in severity from mild to severe.[18] These symptoms may occur within 12–24 hours and can last two to nine days.[19][20][21]
Tests are still being done to get a better understanding of the effects that occur when people become dependent on different forms of caffeine to make it through the day. There has been research findings that suggest that the circadian cycle is not significantly changed under popular practices of caffeine consumption in the morning and during the afternoon.[22]
Children and teenagers
According to the American Academy of Pediatrics (AAP), it is not recommended for individuals under the age of 18 to consume several caffeinated drinks in one day.[23] Failure to restrict caffeine intake can lead to side effects such as increase in heart rate and blood pressure, sleep disturbance, mood swings, and acid reflux.; caffeine's lasting effects on children's nervous and cardiovascular systems are currently unknown. Some research has suggested that caffeinated drinks should not be advertised to children as a primary audience.[24][25]
Pregnancy
If pregnant, it is recommended not to consume more than 200 mg of caffeine a day (though this is relative to the pregnant woman's weight).[26] If a pregnant woman consumes high levels of caffeine, it can result in low birth weight due to loss of blood flow to the placenta,[27] and could lead to health problems later in the child's life.[28] It can also result in premature labor, reduced fertility, and other reproductive issues. The American Pregnancy Association suggests "avoiding caffeine as much as possible" before and during pregnancy or discussing how to curtail dependency with a healthcare provider.[29]
Treatment
Understanding effective treatment strategies is crucial in managing caffeine dependence, a condition that has garnered increasing attention in recent years. A plethora of studies have surfaced aimed at reducing caffeine intake and alleviating withdrawal symptoms. One significant contribution comes from a comprehensive review and research agenda that undertook a thorough examination of caffeine use disorder.[20] This review not only discusses potential diagnostic criteria but also highlights the far-reaching implications for individuals struggling with caffeine dependency. The author characterizes caffeine as a widely consumed substance, yet one that is not immune to fostering dependency. Despite its generally recognized safety profile, clinical evidence suggests a concerning trend wherein users develop a reliance on caffeine, often struggling to curtail consumption despite recurring health concerns, such as cardiovascular issues and perinatal complications.[30]
Evidence-based treatment strategies offer hope for individuals seeking to break free from caffeine dependency. These strategies encompass a spectrum of approaches, including dose tapering, intermittent fasting, diligent monitoring of caffeine intake through journaling, and the incorporation of regular exercise coupled with professional counseling.[20]
Dose tapering
One effective approach to managing caffeine dependence is dose tapering, where caffeine intake is reduced over time. This method allows the body to adjust to lower levels of caffeine gradually, minimizing withdrawal symptoms and discomfort. A study published in the Journal of Caffeine Research demonstrates the efficacy of dose tapering in reducing caffeine consumption among habitual users. Participants who followed a tapering schedule experienced fewer withdrawal symptoms and were more successful in reducing their overall caffeine intake compared to those who abruptly stopped caffeine consumption.[20]
Intermittent fasting
Intermittent fasting, a dietary regimen that involves alternating periods of eating and fasting, has emerged as a potential strategy for managing caffeine dependence. Research suggests that intermittent fasting may help regulate caffeine intake by creating structure periods of abstaining from caffeine consumption. Additionally, intermittent fasting has been associated with improved metabolic health and cognitive function, which may support individuals in overcoming caffeine dependence.[20]
Professional counseling
Seeking professional counseling or therapy can also be beneficial for individuals struggling with caffeine dependence. Counseling sessions provide a supportive environment for individuals to explore the underlying reasons for their caffeine consumption habits and develop coping strategies to manage cravings and withdrawal symptoms. Cognitive behavioral therapy (CBT), in particular, has shown promise in treating substance use disorders, including caffeine dependence. A meta-analysis published in the Journal of Consulting and Clinical Psychology found that CBT interventions were effective in reducing caffeine consumption and improving psychological outcomes among individuals with caffeine dependence.[citation needed]
Regular exercise
Regular physical exercise has been shown to have numerous benefits for overall health and well-being, including aiding in the management of caffeine dependence. Engaging in regular exercise can help individuals reduce stress, improve mood, and promote better sleep quality, all of which may contribute to reducing reliance on caffeine as a stimulant.
It is important that while many adults consume caffeine on a daily basis, withdrawal symptoms may not manifest until 12–24 hours after cessation and can persist for as long as 2–9 days. Such symptoms can significantly impact daily functioning, giving rise to fatigue, headaches, irritability, nausea, mood fluctuations, flu-like symptoms, and dizziness.[31]
^ abcMalenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 16: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN978-0-07-182770-6. Addictive drugs are rewarding and reinforcing because they act in brain reward pathways to enhance either dopamine release or the effects of dopamine in the NAc or related structures, or because they produce effects similar to dopamine. ... Long-term caffeine use can lead to mild physical dependence. A withdrawal syndrome characterized by drowsiness, irritability, and headache typically lasts no longer than a day. True compulsive use of caffeine has not been documented, and, consequently, these drugs are not considered addictive.
^Miller PM (2013). "Chapter III: Types of Addiction". Principles of addiction comprehensive addictive behaviors and disorders (1st ed.). Elsevier Academic Press. p. 784. ISBN9780123983619. Astrid Nehlig and colleagues present evidence that in animals caffeine does not trigger metabolic increases or dopamine release in brain areas involved in reinforcement and reward. A single photon emission computed tomography (SPECT) assessment of brain activation in humans showed that caffeine activates regions involved in the control of vigilance, anxiety, and cardiovascular regulation but did not affect areas involved in reinforcement and reward.
^Sturgess JE, Ting-A-Kee RA, Podbielski D, Sellings LH, Chen JF, van der Kooy D (2010). "Adenosine A1 and A2A receptors are not upstream of caffeine's dopamine D2 receptor-dependent aversive effects and dopamine-independent rewarding effects". Eur. J. Neurosci. 32 (1): 143–54. doi:10.1111/j.1460-9568.2010.07247.x. PMC2994015. PMID20576036. the D1 receptor is not involved in the rewarding effects of caffeine. ... The current data indicates that caffeine has aversive effects at high doses and neither rewarding nor unpleasant effects at low doses. Previous work in rats has indicated that caffeine induces mild preferences at low doses (Brockwell et al., 1991; Bedingfield et al., 1998; Patkina & Zvartau, 1998) and aversions at high doses ... Indeed the rewarding effects of caffeine seen by Brockwell et al.(1991) were at one dose and small. This is similar to our current data; the lower doses of caffeine on our dose-response curve are weakly, but non-significantly rewarding. Also consistent, the rewarding effects of caffeine in humans are mild or absent in individuals with limited caffeine experience
^Volkow, N D; Wang, G-J; Logan, J; Alexoff, D; Fowler, J S; Thanos, P K; Wong, C; Casado, V; Ferre, S; Tomasi, D (April 2015). "Caffeine increases striatal dopamine D2/D3 receptor availability in the human brain". Translational Psychiatry. 5 (4): e549–. doi:10.1038/tp.2015.46. PMC4462609. PMID25871974. We show a significant increase in D2/D3R availability in striatum with caffeine administration, which indicates that caffeine at doses consumed by humans does not increase DA in striatum. Instead we interpret our findings to indicate that caffeine's DA-enhancing effects in the human brain are indirect and mediated by an increase in D2/D3R levels and/or changes in D2/D3R affinity.
^Froestl, Wolfgang; Muhs, Andreas; Pfeifer, Andrea (14 November 2012). "Cognitive Enhancers (Nootropics). Part 1: Drugs Interacting with Receptors". Journal of Alzheimer's Disease. 32 (4): 793–887. doi:10.3233/JAD-2012-121186. PMID22886028. S2CID10511507.
^Juliano, L. M.; Griffiths, R. R. (2004). "A critical review of caffeine withdrawal: Empirical validation of symptoms and signs, incidence, severity, and associated features". Psychopharmacology. 176 (1): 1–29. doi:10.1007/s00213-004-2000-x. PMID15448977. S2CID5572188.